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The LEDs were obtained that the peak emission wavelength and FWHM were 665 nm and 67 nm at 20 mA, respectively. It exhibited a large blueshift of the EL peak wavelength from 691 nm at 5 mA to 631 nm at 100 mA. In this range, the blue-shifted value was 60 nm. Besides, we realized the single peak emission LEDs without an additional emission. We obtained a light output, forward voltage, and EQE of 0.07 mW, 2.45 V, and 0.19% at 20 mA, respectively. The LEDs exhibited the temperature stability of EL intensity and peak wavelength.

We obtained the EL intensity enhancement by a factor of 1.3 with increasing of n-GaN thickness from 2 to 8 µm. We achieved a light output, forward voltage, FWHM and external quantum efficiency of 0.64 mW, 3.3 V, 59 nm, and 1.6% at 20 mA, respectively. Particularly, the wall plug efficiency was 1.0%, which is comparable with the state-of-the-art InGaN-based red LEDs. The reduction of the in-plane compressive stress by the GaN underlying layers appears to be crucial for enhancing the light output of InGaN-based red LEDs on conventional sapphire substrates.

We investigated the effect of the sidewall passivation by hydrogen plasma on the InGaN green micro-LED performance. Hydrogen passivation deactivates the surface region of p-GaN around the perimeter of the device mesa. Thus, hole injection is suppressed in this region, where etching-caused material degradation results in leakage current, decreasing device efficiency. We have confirmed the hydrogen passivation effect on LED square pixels with sizes of 20 and 100 μm. For smaller LEDs, the reverse leakage current has reduced more than tenfold, and the external quantum efficiency of LEDs was enhanced 1.4-times due to the suppression of the non-radiative recombination.

We report the characterization of a N-polar InGaN layer deposited by metalorganic vapor-phase epitaxy on a ScAlMgO4(0001) (SAM) substrate without a low-temperature buffer layer. The InGaN layer was tensile-strained, and its stoichiometry corresponded to In0.13Ga0.87N. We also present the microstructural observation of the InGaN/SAM interface via integrated differential phase contrast-scanning transmission electron microscopy. The results show that the interface between N-polar InGaN and SAM occurs between the O atoms of the O–Sc SAM surface and the (Ga,In) atoms of InGaN.

Fabrication of indium tin oxide (ITO) was optimized for InGaN-based amber/red light-emitting diodes (LEDs). A radiofrequency sputtering reduced the sheet resistivity of ITO at low pressures, and a subsequent two-step annealing resulted in a low sheet resistivity (below 2×10−4 Ωcm) and high transmittance (over 98%) in the amber and red regions between 590 nm to 780 nm. Double ITO layers by sputtering could form an excellent ohmic contact with p-GaN. Application of the double ITO layers on amber and red LEDs enhanced light output power by 15.6% and 13.0%, respectively, compared to those using ITO by e-beam evaporation.

This study demonstrates the performance improvements of InGaN-based red light-emitting diodes (LEDs) by fabricating micro-holes in the planar mesa. The peak wavelengths of the micro-hole LEDs (MHLEDs) exhibited a blue-shift of around 3 nm compared to the planar LEDs (PLEDs) at the same current density. The lowest full width at half maximum of MHLEDs was 59 nm, which is slightly less than that of the PLEDs. The light output power and external quantum efficiency of the MHLED with a wavelength of 634 nm at 20 mA were 0.6 mW and 1.5%, which are 8.5% higher than those of the PLED.

We herein report the growth of phosphor-free InGaN-based white light-emitting diodes (LEDs) by metalorganic vapor-phase epitaxy. The active region consists of blue and red InGaN quantum wells (QWs). To improve the current injection and generate broadband emission, the V-pit structures in the LEDs were fabricated intentionally before growing the QWs. The monolithic white LEDs emit in the range of 410–770 nm and, by tuning the injection current, can cover correlated color temperature (CCT) values corresponding to warm white, natural white, and cool white. The color-rendering index (CRI) of the white LEDs reaches 88 at an injection current of 10 mA. At an injection current of 30 mA, the white LEDs exhibit the chromaticity coordinates of (0.320 and 0.334) in the Commission Internationale de l'Eclairage 1931 chromaticity diagram, a CRI of 78, and a CCT of 6110 K.

This work investigates the influence of residual stress on the performance of InGaN-based red light-emitting diodes (LEDs) by changing the thickness of the underlying n-GaN layers. The residual in-plane stress in the LED structure depends on the thickness of the underlying layer. Decreased residual in-plane stress resulting from the increased thickness of the underlying n-GaN layers improves the crystalline quality of the InGaN active region by allowing for a higher growth temperature. The electroluminescence intensity of the InGaN-based red LEDs is increased by a factor of 1.3 when the thickness of the underlying n-GaN layer is increased from 2 to 8 μm. Using 8-μm-thick underlying n-GaN layers, 633-nm-wavelength red LEDs are realized with a light-output power of 0.64 mW and an external quantum efficiency of 1.6% at 20 mA. The improved external quantum efficiency of the LEDs can be attributed to the lower residual in-plane stress in the underlying GaN layers.

Here we report InGaN-based red light-emitting diodes (LEDs) grown on ( 2 ¯ 01 ) β-Ga2O3 substrates. AlN/AlGaN strain-compensating layers and hybrid multiple-quantum-well structures were employed to improve the crystalline-quality of the InGaN active region. A bare LED showed that peak wavelength, light output power, and external quantum efficiency were 665 nm, 0.07 mW, and 0.19% at 20 mA, respectively. As its forward voltage was 2.45 V at 20 mA, the wall-plug efficiency was 0.14%. The characteristic temperature of the LEDs was 222 K at 100 mA evaluated from the temperature dependence of electroluminescence.

Highlights • Carboxy terminal region of GATA4 is required for cardiogenesis in Xenopus pluripotent explants and in embryos. • Carboxy terminus of GATA4 interacts with CDK4. • CDK4 enhances transcriptional and cardiogenic activity of GATA4. • GATA4-Tbx5 and GATA4-FOG2 interactions are not required for cardiogenesis., GATA4-6 transcription factors regulate numerous aspects of development and homeostasis in multiple tissues of mesodermal and endodermal origin. In the heart, the best studied of these factors, GATA4, has multiple distinct roles in cardiac specification, differentiation, morphogenesis, hypertrophy and survival. To improve understanding of how GATA4 achieves its numerous roles in the heart, here we have focused on the carboxy-terminal domain and the residues required for interaction with cofactors FOG2 and Tbx5. We present evidence that the carboxy terminal region composed of amino acids 362–400 is essential for mediating cardiogenesis in Xenopus pluripotent explants and embryos. In contrast, the same region is not required for endoderm-inducing activity of GATA4. Further evidence is presented that the carboxy terminal cardiogenic region of GATA4 does not operate as a generic transcriptional activator. Potential mechanism of action of the carboxy terminal end of GATA4 is provided by the results showing physical and functional interaction with CDK4, including the enhancement of cardiogenic activity of GATA4 by CDK4. These results establish CDK4 as a GATA4 partner in cardiogenesis. The interactions of GATA4 with its other well described cofactors Tbx5 and FOG2 are known to be involved in heart morphogenesis, but their requirement for cardiac differentiation is unknown. We report that the mutations that disrupt interactions of GATA4 with Tbx5 and FOG2, G295S and V217G, respectively, do not impair cardiogenic activity of GATA4. These findings add support to the view that distinct roles of GATA4 in the heart are mediated by different determinants of the protein. Finally, we show that the rat GATA4 likely induces cardiogenesis cell autonomously or directly as it does not require activity of endodermal transcription factor Sox17, a GATA4 target gene that induces cardiogenesis non-cell autonomously.

A microarray analysis of vegetal pole sequences in the egg and early Xenopus laevis embryo identified Unigene Xl.14891 as a vegetally localized RNA. Analysis of the Xenopus tropicalis genome showed this Unigene to be localized near the 3' end of the Grip2 (glutamate receptor interacting protein 2) transcription unit. RACE showed that the Unigene represented the 3' UTR of Grip2 mRNA. Grip2 mRNA is present in the mitochondrial cloud of late pre-vitellogenic oocytes and then in the germplasm through oogenesis and early development until tailbud tadpole stages. Interference with Grip2 mRNA translation using two antisense morpholino oligos (MOs) impairs primordial germ cell (PGC) migration to the germinal ridges. Both MOs also inhibit swimming movements of the tailbud tadpole, known to involve glutamate receptors. We conclude that Grip2 has several functions in the embryo, including enabling efficient PGC migration.

Hox genes encode transcription factors that regulate morphogenesis in all animals with bilateral symmetry. Although Hox genes have been extensively studied, their molecular function is not clear in vertebrates, and only a limited number of genes regulated by Hox transcription factors have been identified. Hoxa2 is required for correct development of the second branchial arch, its major domain of expression. We now show that Meox1 is genetically downstream from Hoxa2 and is a direct target. Meox1 expression is downregulated in the second arch of Hoxa2 mouse mutant embryos. In chromatin immunoprecipitation (ChIP), Hoxa2 binds to the Meox1 proximal promoter. Two highly conserved binding sites contained in this sequence are required for Hoxa2-dependent activation of the Meox1 promoter. Remarkably, in the absence of Meox1 and its close homolog Meox2, the second branchial arch develops abnormally and two of the three skeletal elements patterned by Hoxa2 are malformed. Finally, we show that Meox1 can specifically bind the DNA sequences recognized by Hoxa2 on its functional target genes. These results provide new insight into the Hoxa2 regulatory network that controls branchial arch identity. BBSRC grant: (BB/E017355/1); Manchester Academic Health Science Centre; Manchester NIHR Biomedical Research Centre; FCT grant: (PTDC/BIA-BCM/71619/2006); Centro de Biologia do Desenvolvimento grant: (POCTI-ISFL-4-664).

Hox transcription factors control morphogenesis along the head-tail axis of bilaterians. Because their direct functional targets are still poorly understood in vertebrates, it remains unclear how the positional information encoded by Hox genes is translated into morphogenetic changes. Here, we conclusively demonstrate that Six2 is a direct downstream target of Hoxa2 in vivo and show that the ectopic expression of Six2, observed in the absence of Hoxa2, contributes to the Hoxa2 mouse mutant phenotype. We propose that Six2 acts to mediate Hoxa2 control over the insulin-like growth factor pathway during branchial arch development.

A conserved molecular pathway has emerged controlling endoderm formation in Xenopus zebrafish and mice. Key genes in this pathway include Nodal ligands and transcription factors of the Mix-like paired homeodomain class,Gata4-6 zinc-finger factors and Sox17 HMG domain proteins. Although a linear epistatic pathway has been proposed, the precise hierarchical relationships between these factors and their downstream targets are largely unresolved. Here, we have used a combination of microarray analysis and loss-of-function experiments to examine the global regulatory network controlling Xenopus endoderm formation. We identified over 300 transcripts enriched in the gastrula endoderm, including most of the known endoderm regulators and over a hundred uncharacterized genes. Surprisingly only 10% of the endoderm transcriptome is regulated as predicted by the current linear model. We find that Nodal genes, Mixer and Sox17 have both shared and distinct sets of downstream targets, and that a number of unexpected autoregulatory loops exist between Sox17 and Gata4-6, between Sox17 and Bix1/Bix2/Bix4, and between Sox17 and Xnr4. Furthermore, we find that Mixer does not function primarily via Sox17 as previously proposed. These data provides new insight into the complexity of endoderm formation and will serve as valuable resource for establishing a complete endoderm gene regulatory network.